Expression of endothelin 3 by mesenchymal cells of embryonic mouse caecum

MA Leibl, T Ota, MN Woodward, SE Kenny, DA Lloyd… - Gut, 1999 - gut.bmj.com
MA Leibl, T Ota, MN Woodward, SE Kenny, DA Lloyd, CR Vaillant, DH Edgar
Gut, 1999gut.bmj.com
Background Mutations in endothelin 3 (EDN3) and endothelin B receptor (EDNRB) genes
cause terminal colonic aganglionosis in mice, and mutations in these genes have also been
linked to the terminal aganglionosis seen in human Hirschsprung's disease. However,
details of EDN3 expression during embryogenesis are lacking, and consequently the
cellular mechanism by which EDN3 regulates innervation of the terminal gut is unclear. Aims
To localise the expression of EDN3 and EDNRB in the embryonic mouse gut. Methods …
Background
Mutations in endothelin 3 (EDN3) and endothelin B receptor (EDNRB) genes cause terminal colonic aganglionosis in mice, and mutations in these genes have also been linked to the terminal aganglionosis seen in human Hirschsprung’s disease. However, details of EDN3 expression during embryogenesis are lacking, and consequently the cellular mechanism by which EDN3 regulates innervation of the terminal gut is unclear.
Aims
To localise the expression of EDN3 and EDNRB in the embryonic mouse gut.
Methods
Expression of EDN3 and EDNRB mRNA was analysed by reverse transcription polymerase chain reaction and in situ hybridisation.
Results
High levels of EDN3 mRNA expression were restricted to mesenchymal cells of the caecum before and after the arrival of neural crest cells. In contrast, EDNRB expression along the gut displayed a time dependent pattern similar to those of the protein tyrosine kinase ret and the neural crest cell marker PGP9.5.
Conclusions
Mesenchymal cells of the caecum express high levels of EDN3 mRNA during embryogenesis and hence the production of EDN3 at the caecum is likely to act on neural crest cells as a paracrine factor necessary for subsequent innervation of the terminal gut.
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